Relevant bibliographies by topics / Platelet factor 4

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Academic literature on the topic 'Platelet factor 4'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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Journal articles on the topic "Platelet factor 4"

Shimizu, T., Y. Ishikawa, Y. Morishima, T. Fukuda, and K. Kato. "Platelet factor 4 release from the platelets stored in platelet concentrates." Transfusion 25, no. 5 (September 1985): 420–23. http://dx.doi.org/10.1046/j.1537-2995.1985.25586020114.x.

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CAPITANIO, A., S. NIEWIAROWSKI, B. RUCINSKI, G. TUSZYNSKI, C. CIERNIEWSKI, D. HERSHOCK, and E. KORNECKI. "Interaction of platelet factor 4 with human platelets." Biochimica et Biophysica Acta (BBA) - General Subjects 839, no. 2 (April 17, 1985): 161–73. http://dx.doi.org/10.1016/0304-4165(85)90033-9.

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O'Brien, J. R. "PLATELET FACTOR 4 (PF 4) AND THE PLATELET MEMBRANE." Acta Medica Scandinavica 191, S525 (April 24, 2009): 65–66. http://dx.doi.org/10.1111/j.0954-6820.1972.tb05793.x.

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Sottile, Jane, Deane F. Mosher, Jan Fullenweider, and James N. George. "Human Platelets Contain mRNA Transcripts for Platelet Factor 4 and Actin." Thrombosis and Haemostasis 62, no. 04 (1989): 1100–1102. http://dx.doi.org/10.1055/s-0038-1647125.

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SummaryRNAs from a number of cells, including platelets, were analyzed by Northern blotting for the presence of transcripts to four platelet proteins - actin, thrombospondin, fibronectin, and platelet factor 4. RNA from platelets contains considerable amounts of mRNA for platelet factor 4, easily detectable mRNA for actin, and traces of mRNA for thrombospondin. mRNA for platelet factor 4 was not detected in human lymphocytes or in any of 5 human cell lines.

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Cowan, S. W., E. N. Bakshi, K. J. Machin, and N. W. Isaacs. "Binding of heparin to human platelet factor 4." Biochemical Journal 234, no. 2 (March 1, 1986): 485–88. http://dx.doi.org/10.1042/bj2340485.

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Platelet factor 4 is a small protein (Mr 7756) from the alpha-granules of blood platelets which binds strongly to and neutralizes the anticoagulant properties of heparin. From an analysis of X-ray crystallographic data a model for the binding of platelet factor 4 to heparin is proposed.

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Dickhout, Annemiek, Bibian M. E. Tullemans, Johan W. M. Heemskerk, Victor L. J. L. Thijssen, Marijke J. E. Kuijpers, and Rory R. Koenen. "Galectin-1 and platelet factor 4 (CXCL4) induce complementary platelet responses in vitro." PLOS ONE 16, no. 1 (January 7, 2021): e0244736. http://dx.doi.org/10.1371/journal.pone.0244736.

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Galectin-1 (gal-1) is a carbohydrate-binding lectin with important functions in angiogenesis, immune response, hemostasis and inflammation. Comparable functions are exerted by platelet factor 4 (CXCL4), a chemokine stored in the α-granules of platelets. Previously, gal-1 was found to activate platelets through integrin αIIbβ3. Both gal-1 and CXCL4 have high affinities for polysaccharides, and thus may mutually influence their functions. The aim of this study was to investigate a possible synergism of gal-1 and CXCL4 in platelet activation. Platelets were treated with increasing concentrations of gal-1, CXCL4 or both, and aggregation, integrin activation, P-selectin and phosphatidyl serine (PS) exposure were determined by light transmission aggregometry and by flow cytometry. To investigate the influence of cell surface sialic acid, platelets were treated with neuraminidase prior to stimulation. Gal-1 and CXCL4 were found to colocalize on the platelet surface. Stimulation with gal-1 led to integrin αIIbβ3 activation and to robust platelet aggregation, while CXCL4 weakly triggered aggregation and primarily induced P-selectin expression. Co-incubation of gal-1 and CXCL4 potentiated platelet aggregation compared with gal-1 alone. Whereas neither gal-1 and CXCL4 induced PS-exposure on platelets, prior removal of surface sialic acid strongly potentiated PS exposure. In addition, neuraminidase treatment increased the binding of gal-1 to platelets and lowered the activation threshold for gal-1. However, CXCL4 did not affect binding of gal-1 to platelets. Taken together, stimulation of platelets with gal-1 and CXCL4 led to distinct and complementary activation profiles, with additive rather than synergistic effects.

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Day, H. James, H. Stormorken, and H. Holmsen. "Subcellular Localization of Platelet Factor 3 and Platelet Factor 4." Scandinavian Journal of Haematology 10, no. 4 (April 24, 2009): 254–60. http://dx.doi.org/10.1111/j.1600-0609.1973.tb00069.x.

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Leavitt, Andrew D. "What for platelet factor 4?" Blood 110, no. 4 (August 15, 2007): 1090. http://dx.doi.org/10.1182/blood-2007-05-091363.

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Robinson, C. "Recombinant Human Platelet Factor 4." Drugs of the Future 20, no. 2 (1995): 148. http://dx.doi.org/10.1358/dof.1995.020.02.284334.

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Lorenz, R., and M. Brauer. "Platelet factor 4 (PF 4) in septicaemia." Infection 16, no. 5 (September 1988): 273–76. http://dx.doi.org/10.1007/bf01645070.

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Dissertations / Theses on the topic "Platelet factor 4"

Brousseau-Nault, Mathieu. "Chronic periodontitis is associated with platelet factor 4 (PF4) secretion." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59016.

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Aim: Platelets contribute to chronic inflammation but their role in periodontitis is not well understood. The aim of this study was to compare platelet recruitment and activation in healthy and inflamed periodontium. Materials and Methods: Gingival crevicular fluid (GCF) samples were obtained from sites of healthy periodontium, gingivitis and periodontitis. Platelets were quantified in the GCF by staining and microscopy. GCF concentrations of platelet factor 4 (PF4) [PF4]GCF and glycoprotein IIbIIIa ([GPIIbIIIa]GCF) were determined by ELISA. Blood samples were obtained from the 3 patient groups. Platelets were isolated from whole blood and stimulated with lipopolysaccharide (LPS) from P. gingivalis to evaluate and compare the LPS-induced PF4 release. Results: Compared to controls, platelet recruitment was increased at gingivitis and periodontitis sites, based on platelet counts and [GPIIbIIIa]GCF. [PF4]GCF was elevated in periodontal pockets but not at gingivitis or healthy sites. Circulating plasma levels of PF4 were higher in patients with generalized severe periodontitis (SP), compared to patients with gingivitis or healthy periodontium. Platelets isolated from SP patients contained and released more PF4 in response to P. gingivalis LPS than platelets from gingivitis or periodontally healthy patients. Conclusions: Periodontitis is associated with increased platelet activation and PF4 release, both locally and systemically.
Dentistry, Faculty of
Graduate

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Javaid, Mohammad. "Platelet factor 4 upregulates matrix metalloproteinase-1 production in gingival fibroblasts." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60244.

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Background and Objective: Periodontitis is a highly prevalent chronic inflammatory disease that causes tooth loss, morbidity and confers an increased risk for systemic disease. Tissue destruction during periodontitis is due in large part to collagen-degrading matrix metalloproteinases (MMPs) released by resident cells of the periodontium in response to pro-inflammatory cytokines. Platelets are immune-competent blood cells with a newly recognized role in chronic inflammation, however their role in the pathogenesis of periodontitis is undefined. Consequently, the objective of this study was to assess the effect of platelet factor 4 (PF4), a major platelet-derived cytokine, on MMP-1 (collagenase) expression in human gingival fibroblasts (HGFs). Methods: HGFs were cultured in the presence or absence of recombinant PF4. Pro-MMP-1 secretion was quantified by enzyme-linked immunosorbent assay (ELISA) analysis of the cell culture supernatants. MMP-1 transcription was quantified by real-time polymerase chain reaction (qPCR). Regulation of MMP-1 production by the p44/42 MAP kinase (MAPK) signaling pathway was examined in the presence or absence of PF4. Results: Exposure to PF4 caused a ~2-3-fold increase in MMP-1 transcription and secretion from cultured human gingival fibroblasts (HGFs). PF4 treatment also enhanced phosphorylation of p44/42 MAP kinase (MAPK), which has been previously shown to induce MMP-1 expression in fibroblasts. Blockade of p44/42 MAPK signaling with the cell-permeant inhibitors PD98059 and PD184352 abrogated PF4-induced pro-MMP-1 transcription upregulation and release from cultured HGFs. Conclusion: We conclude that platelet factor 4 upregulates MMP-1 expression in human gingival fibroblasts in a p44/42 MAPK-dependent manner. These findings point to a previously unidentified role for platelets in the pathogenesis of periodontal diseases.
Dentistry, Faculty of
Graduate

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Kreimann, Martin [Verfasser]. "Characterization of complexes between platelet factor 4 and heparin / Martin Kreimann." Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1065685513/34.

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Yasuba, Hirotaka. "INCREASED RELEASABILITY OF PLATELET PRODUCTS AND REDUCED HEPARIN-INDUCED PLATELET FACTOR 4 RELEASE FROM ENDOTHELIAL CELLS IN BRONCHIAL ASTHMA." Kyoto University, 1991. http://hdl.handle.net/2433/168713.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである
Kyoto University (京都大学)
0048
新制・課程博士
医学博士
甲第4772号
医博第1273号
新制||医||500(附属図書館)
UT51-91-E143
京都大学大学院医学研究科内科系専攻
(主査)教授三河春樹, 教授泉孝英, 教授大島駿作
学位規則第5条第1項該当

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Rudmann, Sally V. "The effect of twenty minutes of aerobic exercise on in vivo platelet release in moderately trained females : radioimmunoassay of platelet factor 4 beta-thromboglobulin /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487266362337217.

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Charpin, Jean-Marie. "Physiopathologie de la bronchiolite obliterante chez les transplantes pulmonaires : implication de 4 mediateurs profibrosants : tgf-beta, igf-1,et-1 et pdgf." Paris 5, 2000. http://www.theses.fr/2000PA05N104.

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Etherington, Michael Denis. "An investigation into the measurement of plasma intraplatelet platelet factor 4 and beta-thromboglobulin in health and thrombotic disease." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278486.

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Kimmerle, Sabine. "Rapid determination of Anti-Heparin/Platelet factor 4 antibody titers in the diagnosis of Heparin-induced Thrombocytopenia$cSabine Kimmerle." Bern : [s.n.], 2003. http://www.stub.unibe.ch/html/haupt/datenbanken/diss/bestell.html.

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Newman, Peter Michael Pathology UNSW. "Antibody and Antigen in Heparin-Induced Thrombocytopenia." Awarded by:University of New South Wales. Pathology, 2000. http://handle.unsw.edu.au/1959.4/17485.

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Immune heparin-induced thrombocytopenia (HIT) is a potentially serious complication of heparin therapy and is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. Early diagnosis of HIT is important to reduce morbidity and mortality. I developed an enzyme immunoassay that detects the binding of HIT IgG to PF4-heparin in the fluid phase. This required techniques to purify and biotinylate PF4. The fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because, unlike in an ELISA, a clearly defined amount of antigen is available for antibody binding. I was able to detect anti-PF4-heparin IgG in 93% of HIT patients. I also investigated cross-reactivity of anti-PF4-heparin antibodies with PF4 complexed to alternative heparin-like anticoagulants. Low molecular weight heparins cross-reacted with 88% of the sera from HIT patients while half of the HIT sera weakly cross-reacted with PF4-danaparoid (Orgaran). The thrombocytopenia and thrombosis of most of these patients resolved during danaparoid therapy, indicating that detection of low affinity antibodies to PF4-danaparoid by immunoassay may not be an absolute contraindication for danaparoid administration. While HIT patients possess antibodies to PF4-heparin, I observed that HIT antibodies will also bind to PF4 alone adsorbed on polystyrene ELISA wells but not to soluble PF4 in the absence of heparin. Having developed a technique to affinity-purify anti-PF4-heparin HIT IgG, I provide the first estimates of the avidity of HIT IgG. HIT IgG displayed relatively high functional affinity for both PF4-heparin (Kd=7-30nM) and polystyrene adsorbed PF4 alone (Kd=20-70nM). Furthermore, agarose beads coated with PF4 alone were almost as effective as beads coated with PF4 plus heparin in depleting HIT plasmas of anti-PF4-heparin antibodies. I conclude that the HIT antibodies which bind to polystyrene adsorbed PF4 without heparin are largely the same IgG molecules that bind PF4-heparin and thus most HIT antibodies bind epitope(s) on PF4 and not epitope(s) formed by part of a PF4 molecule and part of a heparin molecule. Binding of PF4 to heparin (optimal) or polystyrene/agarose (sub-optimal) promotes recognition of this epitope. Under conditions that are more physiological and sensitive than previous studies, I observed that affinity-purified HIT IgG will cause platelet aggregation upon the addition of heparin. Platelets activated with HIT IgG increased their release and surface expression of PF4. I quantitated the binding of affinity-purified HIT 125I-IgG to platelets as they activate in a plasma milieu. Binding of the HIT IgG was dependent upon heparin and some degree of platelet activation. Blocking the platelet Fc??? receptor-II with the monoclonal antibody IV.3 did not prevent HIT IgG binding to activated platelets. I conclude that anti-PF4-heparin IgG is the only component specific to HIT plasma that is required to induce platelet aggregation. The Fab region of HIT IgG binds to PF4-heparin that is on the surface of activated platelets. I propose that only then does the Fc portion of the bound IgG activate other platelets via the Fc receptor. My data support a dynamic model of platelet activation where released PF4 enhances further antibody binding and more release.

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Libraire, Julie. "Le facteur 4 plaquettaire (PF4/CXCL4) prévient la formation du complexe initial de l’inhibiteur de l’activateur du plasminogène (PAI-1) avec sa cible d’origine tissulaire (t-PA)." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P654.

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Le facteur 4 plaquettaire (PF4/CXCL4) est un tétramère constitué de quatre sous-unités identiques de 7,8 kDa qui est libéré en grande quantité par les plaquettes lors de l’hémostase primaire (ensemble des phénomènes permettant un colmatage initial d’une lésion vasculaire). L’étude de la formation d’un caillot de fibrine en présence de PF4 montre une augmentation de la turbidité finale du caillot : le PF4 modifie le réseau formé. Etant donné que la plupart des acteurs de la fibrinolyse se lie au caillot de fibrine et que le PF4 modifie sa structure, nous avons pensé qu’il serait intéressant de rechercher si le PF4 influençait aussi la fibrinolyse. La lyse d'un caillot est effectuée par la plasmine issue de l'activation du plasminogène par son activateur d’origine tissulaire (t-PA) en présence d’un cofacteur qui n'est autre que la fibrine. Nous avons étudié la lyse de caillots de plasma, obtenus par activation de la cascade de la coagulation, en condition statique et à l'aide d'un modèle de thrombose artérielle (système Chandler loop). Dans les deux cas, une diminution du temps de demi-lyse a été observée en présence de PF4. Cependant, la lyse de caillots préparés par simple ajout de thrombine sur du fibrinogène ne permet pas de retrouver cet effet du PF4. Ceci suggère que l’influence du PF4 sur la structure du caillot n’est pas à l’origine de l’effet sur sa lyse et que le PF4 n’influence pas (ou très peu) l'activation du plasminogène, ainsi que l'activité de la plasmine résultante. Cette hypothèse a été confirmée par l’étude de l’activité amydolytique du t-PA et de la plasmine (quelle soit ajoutée ou générée). En système purifié, les inhibiteurs plasmatiques de la fibrinolyse sont absents. Les deux principaux sont l'inhibiteur de l'activateur du plasminogène de type 1 (PAI-1) et l’α2-antiplasmine (α2-AP). La lyse de caillots préparés à partir de plasma déficient en α2-AP montre une diminution du temps de demi-lyse en présence de PF4 (comme pour le plasma normal), alors qu’avec le plasma dépourvu de PAI-1 le temps de demi-lyse n'est plus influencé. De plus, l’ajout de PAI-1 dans le système purifié entraine une diminution du temps de demi-lyse en présence de PF4. Ceci suggère que le PF4 prévient directement ou indirectement l'inhibition du t-PA par PAI-1. L’étude de la cinétique d'inhibition de l’activité amidolytique du t-PA par le PAI-1, la détermination de la stœchiométrie de cette inhibition, et l’analyse de ces cinétiques par immuno-empreinte montrent que le PF4 est un modulateur de la fibrinolyse qui agit en retardant la formation d'un complexe initial entre le t-PA et le PAI-1. Cette nouvelle fonction du PF4 est cohérente, et vient en complément de celle décrite récemment d’inhibiteur de l'activation du TAFI
Platelet factor 4 (PF4/CXCL4) is a tetramer constituted of four identical 7,8 kDa subunits released in large quantities by platelets during primary heamostasis (allowing initial clogging of a vascular injury). Study of fibrin clot formation in the presence of PF4 shows an increase of the final clot turbidity: PF4 modifies the formed network. Given that most fibrinolysis actors are bound to the fibrin clot and that PF4 modifies its structure we thought it would be interesting to investigate if PF4 also influences fibrinolysis. Clot lysis is performed by plasmin originating from activation of its precursor by tissue plasminogen activator (t-PA) with fibrin itself as cofactor of the reaction. We have studied lysis of plasma clots formed by activation of the coagulation cascade in static condition and in a Chandler loop model mimicking arterial thrombosis. Half-times of lysis decreased in the presence of PF4 in both systems. However, PF4 had no longer detectable influence on the half-time of lysis with clots formed by direct addition of thrombin on purified fibrinogen. Observation suggested that the observed decrease of the half-time of lysis induced by PF4 did not originate from its influence on fibrin clot formation and that PF4 had little effect if any on plasminogen activation or plasmin activity. We confirmed this hypothesis by comparing amydolytic activities of t-PA and plasmin (added or generated through plasminogen activation). In purified system, fibrinolysis inhibitors are absent. The two main inhibitors are plasminogen activator inhibitor-1 (PAI-1) and α2-antiplasmin (α2-AP). Lysis of clots obtained from α2-AP deficient plasma showed a decrease of the half-time of lysis in the presence of PF4 (as in normal plasma), whereas in PAI-1 deficient plasma half-time of lysis was unchanged. Moreover if PAI-1 was added to the purified system, half-time of lysis decreased in the presence of PF4. Observations therefore suggested that PF4 prevented directly or indirectly t-PA inhibition by PAI-1. Kinetics of the amidolytic activity of t-PA inhibition by PAI-1 in the presence or not of PF4, determination of its stoichiometry and Western blot analysis of these inhibition kinetics revealed that PF4 is a fibrinolysis modulator which delays formation of the initial (Michaelis) complex between t-PA and PAI-1. This new feature of PF4 is consistent and complementary with its recently described role as a modulator of TAFI activation

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Books on the topic "Platelet factor 4"

Hsiung, Marilyn S. Mechanisms of D(4) dopamine receptor-mediated platelet-derived growth factor receptor-beta transactivation. 2006.

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Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.

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Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.

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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.

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Book chapters on the topic "Platelet factor 4"

Pepper, D. S., and C. V. Prowse. "Beta-thromboglobulin and platelet factor 4." In ECAT Assay Procedures A Manual of Laboratory Techniques, 21–34. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2992-3_3.

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Ishii, Satoshi. "Platelet-Activating Factor (PAF) in Infectious Diseases." In Bioactive Lipid Mediators, 95–108. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55669-5_7.

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Terashita, Z., M. Kawamura, Y. Imura, and K. Nishikawa. "Possible Involvement of Platelet Activating Factor (PAF) in Tissue Factor Generation and the Pathogenesis of Disseminated Intravascular Coagulation (DIC)." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 58–63. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_10.

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Braquet, Pierre G. "Platelet-Activating Factor and Its Antagonists: Scientific Background and Clinical Applications of Ginkgolides." In Ginkgo Biloba A Global Treasure, 359–69. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-68416-9_27.

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Hirashima, Yutaka, Ryoko Kato, Tomoaki Ohmori, Takeshi Nagahori, Michiharu Nishijima, Shunro Endo, Akira Takaku, and Ken Karasawa. "The Role of Platelet-Activating Factor (PAF) in the Development of Chronic Subdural Hematoma." In Recent Advances in Neurotraumatology, 61–64. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68231-8_10.

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Abe, Mamoru, Masaharu Matsuzaki, Takashi Inoue, Hirotoshi Sano, and Tetsuo Kanno. "Significance of Platelet-Activating Factor (PAF) and PAF — Acethylhydrolase in the Pathogenesis of Chronic Subdural Hematoma." In Recent Advances in Neurotraumatology, 65–68. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68231-8_11.

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Miyazaki, Kohji, Kohji Fukunaga, Iqbal Munir, Hitoshi Okamura, and Eishichi Miyamoto. "Expression of Cyclooxygenase (COX)-2 in Human Endometrial Adenocarcinoma Cell Line HEC-1B: An In Vitro Model of the Expression of COX-2 by Platelet-Activating Factor, Human Chorionic Gonadotropin and Prostaglandin E2, and the Possible Signaling Pathways Involved." In Cell and Molecular Biology of Endometrial Carcinoma, 123–38. Tokyo: Springer Japan, 2003. http://dx.doi.org/10.1007/978-4-431-53981-0_8.

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Morita, Takashi, and Hideko Atoda. "The Structural Characterization of Coagulation Factor IX/Factor X-Binding Protein Isolated from the Venom of Trimeresurus Flavoviridis." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 35–40. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_6.

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Shen, Ming-Ching, Shu-Wha Lin, Pei-Chu Yang, and Chin-Chin Huang. "Studies of Factor VIII Inhibitors in Chinese Hemophilia a Patients." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 49–54. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_8.

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Vanhoutte, P. M. "Endothelium-Derived Vasoactive Factors, Platelets and Coronary Disease." In Coronary Circulation in Physiological and Pathophysiological States, 89–102. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68108-3_6.

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Conference papers on the topic "Platelet factor 4"

Bryckaert, M. C., A. Wasteson, G. Tobelem, F. Rendu, and J. P. Caen. "PLATELET DERIVED GROWTH FACTOR (PDGF) BINDS TO HUMAN PLATELETS AND MODULATES PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643493.

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PDGF which is released during platelet activation like the other ∝ granule components (fibrinogen, F VIII/vWF, PF4) could bind to platelet membrane Following this hypothesis, we have studied the binding of 125I pure human PDGF to washed human platelets activated by collagen. This binding was specific and time dependent and reached a plateau with 20 μg/ml of collagen. With 200 fold excess of unlabeled PDGF, the binding of 125I-PDGF decreased progressively to 10 .whereas unlabeled Epidermal Growth Factor did not compete with 125I-PDGF. Saturation curve and scatchard analysis have shown one class of sites 3,000 sites/cell with an apparent Kd = 10-8 M. The demonstration of PDGF binding to platelets led us to investigate the effects of PDGF on platelet function. PDGF inhibited the aggregation and 14C serotonin release induced by thrombin or collagen. This inhibition was dose dependent and more effective with human PDGF. A total inhibition of collagen-induced platelet aggregation was obtained with 50 ng/ml of human PDGF and 200 ng/ml of porcine PDGF. The aggregation and 14C serotonin release induced by arachidonic acid were not inhibited by PDGF. The metabolism of phosphoinositide was also investigated on washed human platelets prelabeled with 32P orthophosphate. We found that PDGF (200 ng/ml) induced a decrease of 32P associated with phosphatidylinositol 4 biphosphate (72 %) after 3 min, with a parallel increase of 32P-phosphatidylinositol 4 Phosphate (120 %) and 32P-phosphatidylinositol (120 %).In conclusion i) PDGF binds to activated platelets, ii) PDGF inhibits platelet aggregation and secretion, iii) PDGF modifies phosphoinositide metabolism. These results are in favour of a role of PDGF in a negative feed back control of platelet activation.

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Ordinas, A., E. Bastida, M. Garrido, J. Monteagudo, L. de Marco, and R. Castillo. "ASIALO VON WILLEBRAND FACTOR ENHANCES PLATELET ADHESION TO VASCULAR SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644098.

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Native Von Willebrand factor (NvWF) binds to platelets activated by thrombin, ADP or ristocetin, and also supports the adhesion of platelets to subendothelium at high shear rates. In contrast, asialo von Willebrand factor (AvWF) induces platelet aggregation in absence of platelet activators. We investigated the role of AvWF in supporting the adhesion of platelets to rabbit vessel subendothelium under flow conditions at a shear rate of 2000 sec-1 for 5 min using the Baumgartner perfusion system. We also studied the effects of blockage of platelet GPIb or GPIIb/IIIa on platelet adhesion using monoclonal antibodies (Mabs),and we measured the rate of binding of 111I-labeled NvWF and AvWF to subendothelium. Perfusates consisted of washed platelts and red cells resuspended in a 4% human albumin solution to which increasing concentrations of NvWF or AvWF had been added. Platelets interacting with the perfused vessels were evaluated morphometrically using a computerized system. At a concentration of 1.2 /ig/ml the percentage of total coverage surface was 21.3 ± 4.8% and 40.0±14.6%, for NvWF and AvWF, respectively (p<0.01). Addition of either Mab against GPIb (LJlbl) or against GPIIb/IIIa (CP8) to the perfusates, reduced platelet deposition (p <0.01). The rates of binding of 111I-labeled NvWF and AvWF to perfused vessel subendothelium were similar (0.83±0.1μg and 0.95±0.1 μg ,respectively).Our results indicate that AvWF enhances the interaction of washed platelets with the vessel subendothelium under flow conditions. Furthermore, they suggest that this effect is related to the interaction of AvWF with platelets and not to an increased affinity of AvWF for subendothelium.

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Boschetti, C., A. Vicari, E. Cofrancesco, A. Della Volpe, G. Moreo, E. Po-gliani, G. Pozza, and E. Polli. "HEPARIN-RELEASED PLATELET FACTOR 4 (HR-PF4) IN DIABETIC MICR0VAS-CULAR DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643498.

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When heparin is injected i.v. as a bolus, PF4 but not (β-throm boglobulin ((βTG) is released immediately. HR-PF4 is not liberated from platelets but from the endothelial cells of vessels which serve as storage sites. The role of platelet activation in diabetic microvascular disease is still controversial, however there is experimental evidence of vascular injury and hemostatic activation preceding the appearance of microvascular disease. The contradictory results so far obtained in man may be partly attributed to the heterogeneity of the diabetic patients studied. We studied 20 insulin-dependent diabetics (age 21-40) in stable metabolic equilibrium (mean HbAlc=7.6%). 10 without fluoroangiographic evidence of retinopathy (Group l) and 10 with retinopathy (Group 2). None had signs or symptoms of macrovascular disease. The control group consisted of 10 healthy volunteers (age 22-39). No medication except insulin was taken for at least 10 days preceding the study. 12 h before the study all subjects received aspirin 500 mg p.o. Plasma (βTG and PF4 were determined before (basal) and 5,30,90 min after a heparin bolus i.v. (5000 U). Protein C, factor VIIIR:Ag and tissue plasminogen activator were also measured in plasma.

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Bodzenta-Lukaszvk, A., K. Krupiński, and M. Bielawiec. "PLATELET FUNCTION AND KALLIKREIN SYSTEM IN PATIENTS WITH ESSENTIAL HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644258.

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Since the pathogenesis of hypertension is still discussed the aim of this study was to investigate behaviour of platelets and kallikrein system in patients suffering from this disease. In 30 patients with essential hypertension, aged 23-31 years and 20 normotensive healthy subjects, aged 21-35 years the following parameters of platelet function were studied: platelet aggregation induced with ADP,platelet activating factor (PAF) and arachidonic acid (AA) according Born's method, plasma beta-thromboglobulin (Beta-TG) and platelet factor 4 (PF4) , plasma thromboxane B2 (TXB2) and cyclic AMP using radioimmunoassay kits. The activity of kallikrein and factor XII was also determined using Chromo-zym PK (Boehringer Mannheim GmbH). The hypertensive patients demonstrated a greater platelet aggregability by ADP and PAF, elevated concentrations of Beta-TG and TXB2 as well as decreased level of cyclic AMP in comparison to normotensive subjects. No significantly changes in platelet aggregability by AA and activity of PF4 were found in the group of hypertensive patients. There were also significantly decreased plasma concentrations of kallikrein and factor XII in these patients. Obtained results have shown hyperfunction of blood platelets and depletion of kallikrein system in the patients with essential hypertension. These results suggest that among different pathogenic factors function of blood platelets and kallikrein system should be taken into consideration.

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Vigh, Zs, and I. Scharrer. "INVESTIGATIONS ON MULTIMERIC STRUCTURE OF PLATELET VON WILLE-BRAND FACTOR IN PATIENTS WITH HEREDITARY DISORDERS OF PLATELET FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644087.

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Von Willebrand factor (vWF), a multimeric glycoprotein, plays an essential and multifunctional role in the hemostatic process. It is well known that platelet glycoproteins IB, IIB and IIIA contain receptors for vWF. Von Willebrand factor was also found in alpha granules of platelets. Therefore we investigated the multimeric structure of platelet vWF in 12 patients with different inherited disorders of platelet function. The patients had the following diagnosis: Hermansky Pudlak syndrome, Thrombasthenia and up to new undefined hereditary disorders of platelet function. The method is based upon:1) washing of platelets 2) release of platelet vWF 3) separation of vWF multimers by SDS-agarose electrophoresis 4) subsequent blotting of vWF mul timers onto nitrocellulose 5) staining by peroxidase conjugated antibodies.The investigations were repeated 3 times and compared to those of normal platelets. In 2 patients with Hermansky-Pudlak syndrane no multimeric structure could be detected in platelets whereas the multimeric pattern of plasma of these patients was normal. Also in one patient with the tentative diagnosis: thrombasthenia we couldn't find any multimeric structure in platelets compared to the normal multimeric composition of plasma. In 2 patients with giant platelets the multimeric distribution was normal. In the remaining 6 patients we observed multimeric structure which was different from that seen in vWd variants and in healthy volunteers. In 1 patient we found normal multimeric pattern in plasma and platelets.Based on our findings it can be assumed that the analysis of multimeric structure of platelet vWF can be helpful for the diagnostic approach and for the insight in pathogenesis of inherited disorders of platelet function.

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Gewirtz, A., W. Y. Xu, B. Rucinski, and S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.

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Platelet (plt) factor 4 (PF4) is an alpha granule protein which can modulate T lymphocyte function. T cells may help regulate megakaryocytopoiesis. Therefore, we hypothesized that T cell-PF4 interactions might play a role in autoregulating marrow megakaryocyte (MEG) production. To test this idea, we studied MEG colony formation in plasma clot cultures containing human serum derived solely from pit poor normal AB plasma, enriched hematopoietic progenitor cells (HPC), autologous T cells, and exogenous PF4. Highly purified PF4 (single band on SDS gel) was prepared from outdated human pits by a combination of heparin-agarose, Sephacryl G-200, and Sephadex G-50 column chromatography. HPC were prepared by depleting normal light density marrow mononuclear cells of adherent monocytes, and T cells. T cells were further fractionated into helper (Leu 3+) and suppressor (Leu 2+) subtypes by solid phase immunoabsorption ("panning"). MEG colonies were enumerated by indirect immunofluorescence with an anti-human platelet glycoprotein antiserum. HPC(5×105/ml) were co-cultured with Leu 3+, or Leu 2+ T cells at target;T cell ratios of 2:1 (n=3; n=4 respectively) and l:l(n=4; n=4 respectively) in the presence of 2.5 μg/ml PF4. Under these growth conditions, MEG colony formation was unchanged (p>0.5) when compared to colonies formed by HPC in the absence of PF4. When the above experiments were repeated (n=2-3/condition) at a higher PF4 concentration [25 μg/ml], MEG colony formation was markedly (>60%) inhibited. To determine if PF4 directly inhibited MEG or erythroid progenitor cell growth (CFU-Meg; CFU-E) in vitro, HPC were cloned in PF4 (25μg/ml) without added T cells. Mean ± SEM of MEG and CFU-E derived colonies formed without vs. with PF4 was as follows:These results suggest that: 1) PF4 may be a non-T cell dependent, lineage specific inhibitor of CFU-MEG, and 2) PF4 may play a role in autoregulating human megakaryocytopoiesis.

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Rucinski, B., G. J. Stewart, G. Boden, and S. Niewiarowski. "INTERACTION OF PLATELET FACTOR 4 WITH HEPATOCYTES AND ITS POSSIBLE SIGNIFICANCE IN HEMOSTASIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643500.

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Previous experiments have demonstrated the rapid clearance of himan platelet factor 4 (PF4) from rabbit and rat blood, its accumulation in the liver and its elimination of PF4 degradation products with urine. Injection of heparin resulted in a rapid loss of 125 i-pF4-radioactivity from the liver (Rucinski et al Amer. J. Physiol. 251, H800, 1986). Current experiments demonstrate the uptake of human 125i-pf4 by hepatocytes reaching maximum at 180 min. This uptake is 2-3 times greater at 37°C than at 4°C. At 37°C degradation of 125I-PF4 by hepatocytes was also observed as indicated by the increase of 125j_pf4 radioactivity soluble in 6% trichloracetic acid. By contrast, no uptake of 125I-β was observed. Autoradiography demonstrated association of l25I-PF4 with hepatocytes membranes while after longer incubation (20-60 min) radioactivity was also localized in endosanes. The heparin inhibited binding and uptake of PF4 by hepatocytes; accordingly the injection of heparin to or into rabbits within 10 min resulted in a rapid urinary clearance of 125I-PF4 and the injection of PF4 resulted in a rapid urinary clearance of 3H-heparin. We propose that 1) PF4 released to the circulating blood by activated platelets is bound to the surface of hepatocytes and that it is further processed by these cells over time; 2) the presence of PF4 in the liver may contribute to the regulation of hemostasis by neutralizing anticoagulant activity of endogenous heparin-like molecules; 3) in clinical situations PF4 may enhance clearance of injected heparin by accelerating its urinary excretion.

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COEFFIER, e., D. Delautier, J.-P. Le Couedic, M. Chinqnard, and J. Benveniste. "ACTIVATED HUMAN PLATELETS AND NEUTROPHILS COOPERATE FOR THE FORMATION OF PAF-ACETHER (PLATELET-ACTIVATING FACTOR)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642881.

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Interactions between platelets and neutrophils have been reported for the production of several mediators of inflammation such as hydrogen peroxides or leukotrienes. Another potential mediator of thrombosis and inflammation is paf-acether which is synthesized by activated platelets and neutrophils.Since platelets form and release large amounts of the paf-acether precursor lyso paf-acether, platelets and neutrophils cooperation for paf-acether biosynthesis was investigated. Purified human neutrophils (4 × 106 /ml) stimulated by opsonized zymosan (ZC, 1 mg/ml) formed 4.5 ± 2.5 ng/ml paf-acether. Human washed platelets (3 × 108 /ml) stimulated with thrombin (l IU/ml) formed 0.60 ± 0.43 ng/ml paf-acether. Platelets and neutrophils, incubated together and both stimulated by their specific agonist, formed more than twice as much paf-acether as platelets and neutrophils separately (10.90 ± 4.25 ng/ml, n = 6, p < 0.001). The formation of lyso paf-acether and the release of lysozyme and LDH were unchanged under the cooperation conditions. The formation of paf-acether almost doubled(10.24 ± 8.79 ng/ml paf-acether versus 5.30 ± 5.23, p < 0.05, n = 4) when ZC-stimulated neutrophils were incubated with supernatants from thrombin-stimulated platelets as well as with synthetic lyso paf-acether. Extracted and purified lyso paf-acether from thrombin-stimulated platelets led to increase of biosynthesis of paf-acether by neutrophils (13.86 ± 3.92 ng/ml paf-acether versus 5.76 ± 0.66, p < 0.05, n = 3). These results indicate that cooperation between platelets and neutrophils is likely to occur via acetylation by neutrophils of excess lyso paf-acether originating from platelets. Thus neutrophils can increase their biosynthesis of paf-acether by acetylating lyso paf-acether either synthetic or released from other cells.

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Suzuki, Sozo, Kazuo Mori, Koji Sugai, Yasuyuki Akutsu, Masaaki Ishikawa, Hideaki Sakai, and Katsuhide Hiwatashi. "ELECTRONMICROSCOPIC STUDIES ON PLATELETS AND MEGAKARYOCYTES IN GIANT PLATELET SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644560.

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Giant platelet syndrome are characterized morphologically by many giant platelets associated with several functional abnormalities in the peripheral blood. However, the mechanism of large platelet production has not yet been clarified. In 1981, we reported acase with Bernard-Soulier syndrome(BSS) in whom giant platelets were considered to be formed by fusion of two or three platelets in the circulating blood. We examined the ultrastructure of platelets and megakaryocytes in another case with BSS (29 year-old female) and a case with May-Hegglin anomaly (31 year-old male). Whole blood and bone marrow specimens were fixed with glutaraldehyde-osmium solution. Thin sections were prepared and stained with uranyl acetate and lead cytrate. Membrane systems of platelets and megakaryocytes in a case with BSS was investigated by staining of surface coating with ruthenium red.In a case with BSS, most platelets were very large and similar in morphology to those in formerly reported case. Giant platelets contained several-fold increased number of α-granules and mitochondria. Typical dense bodies were also observed. Contents of ATP/ADP, platelet factor-4(PF-4), B-thromboglobulin(B-TG) and platelet factor-3 availability(PF-3) were increased. Disorganization of microtubules was recognized. Some giant platelet contained membrane systems similar to demarcation membranes(DM) in megakaryocytes, characteristically. In mature megakaryocytes, areas divided by DM similar in size to those in normal megakaryocytes were observed. Several of these areas appeared to fuse together to form the giant platelets containing many granules and remnants of DM. In a case with May-Hegglin anomaly, typical Dohle’s bodies were shown in neutrophilic granulocytes. Giant platelets in this case also contained large number of α-granules and some of them contained membrane systems similar to DM. Areas similar in morphology to these giant platelets were clearly noted in the cytoplasm of mature megakaryocytes.In these cases, most giant platelets in the peripheral blood may be formed in the cytoplasm of megakaryocytes by fusion of several areas divided by DM, each of which may become normal sized platelets in normal megakaryocytes.

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Kim, Youngmi, Eunhee Kim, Olga Guryanova, Masahiro Hitomi, Andrew E. Sloan, Anita B. Hjelmeland, and Jeremy N. Rich. "Abstract 5192: Platelet derived growth factor receptors differentially inform intertumoral and intratumoral heterogeneity." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5192.

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